tbuckley/cabot-search huggingface dataset:
Proliferative diabetic retinopathy: treatment with xenon-arc photocoagulation. Interim report of multicentre randomised controlled trial.
Journal: BMJ (1977)

One hundred patients with symmetrical proliferative diabetic retinopathy had one eye randomly chosen for treatment with xenonarc photocoagulation while the other was left untreated as a control. Patients were subdivided into those with new vessels on both optic discs and those with only peripheral new vessels. In patients with new vessels on the optic discs the vision of the untreated eyes deteriorated more than that of the treated eyes and the difference in deterioration was significant after one, two, and three years. There was no such difference in patients who had only peripheral new vessels. Eighteen patients had become blind in one or both eyes by the last assessment, but only one patient became blind in the treated eye without concomitant blindness in the untreated eye. Thirteen were blind only in the untreated eye. Both photographic and ophthalmoscopic examinations showed that new vessels on the disc regressed more in the treated eyes than in the untreated ones. As some forms of diabetic retinopathy are now treatable, early diagnosis and evaluation is increasingly important.
Effects of Medroxyprogesterone Acetate on Gene Expression in Myometrial Explants from Pregnant Women
Authors: Yolande Cordeaux, Mark Tattersall, D. Stephen Charnock-Jones, Gordon C. S. Smith
Journal: Endocrine Reviews (2010)

ContextProgesterone is important physiologically and therapeutically to maintain uterine quiescence during pregnancy, in part through controlling myometrial gene expression.
Staphylococcal Disease
Authors: LEIGHTON E. CLUFF
Journal: Annals of Internal Medicine (1962)

Editorial1 September 1962Staphylococcal DiseaseLEIGHTON E. CLUFF, M.D.LEIGHTON E. CLUFF, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-57-3-499 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe seriousness of staphylococcal disease during the past several years has been largely attributable to the emergence of infections caused by staphylococci resistant to available antibacterial drugs. Recently, however, increasing experience with penicillinase-resistant semisynthetic penicillins, such as methicillin and oxacillin, as reported by Simon and Rantz in this issue of the ANNALS, has provided means for the effective drug treatment of almost all severe staphylococcal disease. Nevertheless, there is no evidence and no reason to expect that these antibiotics will reduce significantly the incidence of staphylococcal infection. It is expected that infection will continue to occur, but severe staphylococcal disease...References1. ROGERS DE: The changing pattern of life-threatening microbial disease. New Engl. J. Med. 261: 677, 1959. CrossrefMedlineGoogle Scholar2. MINCHEWCLUFF BHLE: Studies of the epidemiology of staphylococcal infection. I. Infection in the hospitalized patient. J. Chron. Dis. 4: 354, 1961. CrossrefGoogle Scholar3. KEENEMINCHEWCLUFF WBHLE: Studies of the epidemiology of staphylococcal infection. III. Clinical factors in susceptibility to staphylococcal disease. New Engl. J. Med. 265: 1128, 1961. CrossrefMedlineGoogle Scholar4. WEINSTEIN HJ: The relation between the nasal-staphylococcal-carrier state and the incidence of postoperative complications. New Engl. J. Med. 260: 1303, 1959. CrossrefMedlineGoogle Scholar5. KNIGHTWHITEFOSTERWENZEL VAFT: Studies on staphylococci from hospital patients. II. Effect of antimicrobial therapy and hospitalization on carrier rates. Ann. N. Y. Acad. Sci. 65: 206, 1956. CrossrefMedlineGoogle Scholar6. BERNTSENMCDERMOTT CAW: Increased transmissibility of staphylococci to patients receiving an antimicrobial drug. New Engl. J. Med. 262: 637, 1960. CrossrefMedlineGoogle Scholar7. OTTENHEIMERMINCHEWCOHENCLUFF EJBHLSLE: Studies of the epidemiology of staphylococcal infection. II. Isolation of staphylococci from the milk of nursing mothers under non-epidemic conditions. Bull. Johns Hopkins Hosp. 109: 114, 1961. MedlineGoogle Scholar8. COHEN LS: Unpublished data. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Medicine Johns Hopkins University School of Medicine Baltimore 5, Maryland PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCELLULAR REACTIONS IN THE PATHOGENESIS OF STAPHYLOCOCCAL INFECTION* 1 September 1962Volume 57, Issue 3Page: 499-501KeywordsAntibioticsDrugsInfectious diseasesPenicillinStaphylococcal infection Issue Published: 1 September 1962 PDF downloadLoading ...
Cover Image, Volume 39, Issue 5
Authors: Dan Li, Wenfang Zhou, Jinping Pang, Qin Tang, Bingling Zhong, Chao Shen, Li Xiao, Tingjun Hou
Journal: Medicinal Research Reviews (2019)

Description of the front cover image: The cover image is based on the Review Article A magic drug target: Androgen receptor by Dan Li et al., https://doi.org/10.1002/med.21558.
Documented hypoglycemia for 23 years in a patient with insulinoma
Authors: R. L. Nelson
Journal: JAMA (1978)

IT IS well known that the diagnosis of insulinoma may be delayed because of the variable presentation of symptomatic hypoglycemia. Hypoglycemic symptoms were present for more than three years in 38% of 154 patients seen at the Mayo Clinic from 1927 to 1964<sup>1</sup>and in 15 of 60 patients seen there from 1964 to 1975.<sup>2</sup>Twenty-five percent of 258 patients reported in the world literature up to 1949<sup>3</sup>had symptoms for more than five years before operative intervention. Documentation of hypoglycemia generally follows the onset of symptoms by some time. The longest period of documented hypoglycemia that we could locate in the literature was 15 years.<sup>3</sup> We recently noted hyperinsulinemia in a patient who has had symptoms compatible with fasting hypoglycemia for more than 50 years and in whom hypoglycemia had been demonstrated 23 years previously. <h3>Report of a Case</h3> A 74-year-old woman was seen at the
Epidemiology of congenital rubella syndrome. The role of maternal parity
Authors: S. C. Schoenbaum
Journal: JAMA (1975)

Rubella vaccination policies are primarily directed at control of congenital rubella syndrome. In the United States, vaccination of children of both sexes, ages 1 through 12 years, has been recommended. This policy depends on the hypothesis that children are the major source of infection for pregnant women. If true, then as maternal parity increases one would expect an increasing prevalence of rubella antibody or an increase in the frequency of rubella syndrome in babies. A serologic survey of 3,081 pregnant women has failed to show an increase in prevalence of rubella antibody with increasing parity. Case-control studies comparing groups of children with rubella syndrome to birth certificate and hospital control groups also have failed to show an excess of multiparae among the mothers of babies with rubella syndrome. Thus, these results do not support the hypothesis that children are the major source of infection for pregnant women. (<i>JAMA</i>233:151-155, 1975)
ACTR-09. TARGETING MYELOID DERIVED SUPPRESSOR CELLS: PHASE 0/1 TRIAL OF LOW DOSE CAPECITABINE + BEVACIZUMAB IN PATIENTS WITH RECURRENT GLIOBLASTOMA
Authors: David Peereboom, Justin Lathia, Tyler Alban, Alireza Mohammadi, Manmeet Ahluwalia, Cathy Brewer, Michael Vogelbaum
Journal: Neuro-Oncology (2018)

Glioblastoma (GBM) creates an immunosuppressive environment that allows tumor growth. Myeloid derived suppressor cells (MDSCs) mediate immunosuppression in GBMs. MDSCs are up-regulated in the blood of GBM patients. We have developed a novel strategy to target GBM immunosuppression using low dose 5-fluorouracil (5-FU) to target MDSCs. Marked MDSC depletion occurs at 5-FU doses in mice equivalent to <10% of the normal human dosing. Goal: proof of concept that MDSC suppression is feasible in GBM patients with low-dose capecitabine [cap], (oral 5-FU analogue). Eligibility: Recurrent GBM in need of surgical resection; no prior cap or bevacizumab. Cohorts of 3–6 patients receive low-dose cap 150 mg/m2/d (dose level 1) for 7 days pre-surgery. Post-op, patients resume cap for one cycle after which bev is added. Concentrations of blood MDSCs, immune cells, and relevant secreted factors are measured at baseline; pre- and post-op; and after the addition of bev. Tumors are assayed for MDSCs and glioma stem-like cells (GSCs). Primary endpoint: MDSC and T-regulatory cell (T-reg) reduction after cap. Seven patients have enrolled to date. In all patients MDSCs rose initially after resection (max rise 18% over baseline) and subsequently began to fall after cycle 2 (max reduction 6%). T-regs fell slightly (0–12%) in 5 of 7 patients. Cytotoxic T-cell (CTL) concentrations rose significantly (max 93%). CD3+ T-cells fell in 5 of 7 patients (max reduction 52%). Four of 7 (71%) of patients reached PFS6. Median PFS-6 months (2–14 mos). Median overall survival 10 months (5–16). Treatment-related SAEs: grade 3 dyspnea; grade 2 hemorrhage, non-neutropenic fever; and grade 1 hand-foot. Low-dose capecitabine is associated with a modest reduction in MDSCs and T-regs and a significant increase in CTLs. Toxicity has been manageable. Four of 7 evaluable patients have reached 6 months free of progression. Dose escalation continues.
ON THE COVERThe Rise of Direct-to-Consumer Advertising of Prescription Drugs in the United StatesRethinking the Role of the Learned Intermediary: The Effect of Direct-to-Consumer Advertising on LitigationChallenges in Regulating Direct-to-Consumer AdvertisingGifts to Physicians in the Consumer Marketing EraDirect-to-Consumer Advertising of Prescription Drugs: Implications for the Patient-Physician Relationshipit was too soon when I went downGrandpa
Journal: JAMA (2000)
Invasive pneumococcal disease among children in a health district of Barcelona: early impact of pneumococcal conjugate vaccine
Authors: E. Calbo, Á. Díaz, E. Cañadell, J. Fábrega, S. Uriz, M. Xercavins, M. A. Morera, E. Cuchi, M. Rodríguez-Carballeira, J. Garau
Journal: Clinical Microbiology and Infection (2006)
CompLEEment-1: phase 3b study of ribociclib + letrozole for the treatment of hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2–) advanced breast cancer (ABC) in patients with no prior endocrine therapy (ET) for ABC
Authors: C. Zamagni, M. Martin, A. Ring, P. Cottu, K. Zhou, J. Wu, J.P. Zarate, M. De Laurentiis
Journal: Annals of Oncology (2017)
Health Status Among Hispanics: Major Themes and New Priorities
Authors: Antonio Furino
Journal: JAMA (1991)

In late 1989, a national forum was convened to bring together about 100 of the nation's most experienced researchers and administrators who are actively involved in studying and improving the health status of Hispanics.<sup>1,2</sup>The purpose of that meeting was to draft a clear policy and research agenda that, if followed, could effectively solve health problems affecting the Hispanic population. Much of the research on Hispanic health now in progress could be directly or indirectly related to the attendees at the forum. That accounted for a productive exchange of information among participants and, at the same time, reflected a serious deficiency—given the magnitude and the scope of the health problems facing Hispanics, too few scholars and researchers are engaged in clarifying and solving them. A few explanations may be offered for the present state of the art. National data sets on health status, such as those compiled through the
PROGRESS IN MEDICAL EDUCATION.
Journal: JAMA (1894)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
BEARERS OF BACTERIAL BURDENS
Journal: JAMA (1967)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
HGG-18. MOLECULAR PATHOPHYSIOLOGY OF HISTONE G34R MUTANT CHILDHOOD BRAIN TUMOURS; TOWARDS THE DEVELOPMENT OF NOVEL TARGETED THERAPIES
Authors: Farhana Haque, Anbarasu Lourdusamy, Ruman Rahman, Pascale Varlet, Angel Carcaboso, Chris Jones, Robert Layfield, Richard Grundy
Journal: Neuro-Oncology (2018)

There have been no recent improvements in the treatments for childhood and adolescent High-Grade Glioma (pHGG) and Diffuse Intrinsic Pontine Glioblastoma (DIPG) which continue to have a very poor prognosis (<25%). These cancers are defined by mutations affecting histone 3 proteins, indeed 80% of DIPGs harbour histone H3.1 and H3.3 K27M somatic mutations whilst 30% of pHGGs exhibit H3.3 G34R or G34V mutations. Several studies have highlighted the epigenetic changes associated with these mutations, however their precise role in tumourigenesis is still unknown. We have generated and validated a Histone 3.3 (H3.3) G34R antibody and investigated the downstream effects of H3.3 G34R mutations in pHGG. In order to identify the genes that may be deregulated by mutant histone expression, we have performed chromatin immunoprecipitation (ChIP) assays with our H3.3 G34R and wild type H3 antibodies, using pHGG mutant and wild type cell lines. Initial analyses of ChIP data have implicated deregulation of various cell signaling pathways including as Notch, Hedgehog, PAR-1, PLC-beta and Androgen, in H3 G34R mutated pHGG. Specifically, Notch pathway genes e.g. HES1/HES5 were found enriched at promoter regions by the H3.3 G34R antibody in mutant cell lines. We are currently determining the effects of altered expression or inhibition of Notch pathway components on tumorigenesis of H3 G34R mutated pHGG, through protein/gene expression and inhibition assays. These analyses should enable us to find potential novel therapeutic targets. Results of these initial analyses/experiments will be presented.
Abdominal Surgery
Authors: Claude E. Welch, Ronald A. Malt
Journal: New England Journal of Medicine (1979)

(Third of Three Parts)PancreasDiagnostic MethodsTwo papers from the University of Chicago compared available methods for detection and diagnosis of a pancreatic mass. In the first, the overall comparative accuracy was 88 per cent with endoscopic retrograde cholangiopancreatography, 72 per cent with ultrasound, 64 per cent with scans and 64 per cent with angiography.176 In the second, computerized tomography had been used and showed promise.177 Ultrasound is the primary diagnostic method since it is simple, noninvasive and comfortable for the patient and has a high probability of success. In the Massachusetts General Hospital experience, computerized tomography is best . . .
Step care for asthma
Authors: R. C. Bone
Journal: JAMA (1988)

Asthma has classically been considered a disease characterized primarily by bronchospasm. In addition to bronchospasm, however, the pathologic characteristics of severe asthma include bronchial inflammation, consisting of lymphocytic and eosinophilic infiltration, as well as desquamation of ciliated epithelium. In fact, it has been proposed that asthma be renamed "chronic desquamative eosinophilic bronchitis."<sup>1</sup> Despite recent advances in the therapy for bronchial asthma, the morbidity and mortality associated with this disease are increasing,<sup>2</sup>with concomitant increases in the sale of bronchodilator medications.<sup>3</sup>Although the explanation of this disturbing trend is unknown, investigators and clinicians are reevaluating current concepts of asthma pathophysiologic characteristics and treatment, particularly the prevention and control of bronchial inflammation. To reverse the increased death rate in patients with asthma, treatment of bronchospasm must be combined with the control of chronic desquamative eosinophilic bronchitis.<sup>1</sup>Step-care treatment of asthma should be strongly considered as an approach to
Abstract 17066: Cellular Repressor of E1A-Stimulated Genes Protects From Myocardial Ischemia/Reperfusion Injury by Regulating Myocardial Autophagy and Apoptosis
Authors: Chenghui Yan, Haixu Song, Xiaoxiang Tian, Yang Li, Guitang Yang, Chengfei Peng, Mingyu Sun, Yaling Han
Journal: Circulation (2015)

Background: Cellular repressor of E1A-stimulated genes (Creg) is a secreted glycoprotein that regulates tissue and cell homeostasis and has been shown to antagonize heart injury; however, little is known about the role of CREG in ischemia/reperfusion injury (IRI). In this study, we aimed to investigate the role of CREG in cardiac IRI and clarify the mechanism. Methods: Myocardial ischemia/reperfusion (MIR) was established by ligation of left descending coronary artery for 30 min in wild type C57 mice (Creg+/+) and heterozygous Creg mice (Creg+/–). Expression of CREG was determined by Western Blot. Infarction size was determined by TTC and Evan’s Blue staining 24 hours after MIR. Cardiac function was evaluated by echocardiography at day 28. Recombinant CREG protein (0.3mg/kg·d) was supplemented through micro-pump embedded subcutaneously in Creg+/+ mice. Cardiac function and infarction size were assessed as mentioned above. Apoptosis, lysosome formation and function were detected in both heart tissue and cardiomyocyte cell line H9C2. Results: Level of CREG protein in mouse hearts was downregulated after mice were subjected to MIR, especially in Creg+/– mice. Creg+/– mice had larger infarction sizes after 24 hours of MIR treatment and worse cardiac function at day 28 compared with Creg+/+ mice. However, cardiac function was significantly improved in Creg+/+ mice treated with recombinant CREG protein. In Creg+/– mice, the number of cardiomyocytes undergoing apoptosis was increased, and LC3A and p62 accumulated, suggesting that autophagy was dysfunctional. Upregulation of CREG decreased apoptosis and activated autophagy of cardiomyocytes. Furthermore, we demonstrated that CREG protects cardiomyocytes against apoptosis by activating autophagy both in vivo and in vitro. Conclusions: CREG overexpression protects cardiac function against IRI by preventing cardiomyocyte apoptosis. The protective effects of CREG are partly mediated by activation of lysosomal autophagy.
AB0111 Role of Toll-Like Receptor 9 in the Pathogenesis of Inflammatory Autoimmune Arthritis and Osteoclast Activation
Authors: A. Fischer, C. Böhm, V. Saferding, E. Goncalves-Alves, R. Kreindl, M. Koenders, W. van den Berg, T. Rothe, G. Krönke, D. Dudziak, G. Steiner
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> There is some evidence that release and insufficient removal of endogenous nucleic acids may be involved in triggering harmful autoimmune reactions that might be important in the initiation of RA. Nucleic acid-sensing molecules, such as the endosomal Toll-like receptors (TLRs) 7 and 9, have been linked to pathogenic autoimmune processes, particularly in SLE, but their role in RA is less clear. Data recently obtained in rats with pristane-induced arthritis (PIA) suggested involvement of TLR9, because antagonizing this receptor in the initiation phase of the disease led to an improved clinical outcome of arthritis. <h3>Objectives</h3> To gain more insight into the role of TLR9 in autoimmune arthritis we have extended our studies to the K/BxN serum-transfer arthritis model which is reflecting the effector phase of erosive autoimmune arthritis. <h3>Methods</h3> Arthritis was induced in C57BL/6 mice by two subsequent injections of arthritogenic serum. Antagonists for TLR7 and TLR9 or an agonist for TLR9, respectively, a non-inhibitory control sequence or PBS as placebo was applied every third day. The first treatment was given one day before disease induction. To further investigate TLR9 involvement, arthritis was also induced in TLR9 knock-out mice. Furthermore, the effect of TLR9 on osteoclast differentiation and activation was investigated in an <i>in vitro</i> osteoclast formation assay. <h3>Results</h3> Neither inhibitor affected arthritis onset and severity in the serum transfer model, which is independent of the adaptive immune system, in contrast to PIA. Furthermore, arthritis severity was not changed in mice lacking a functional tlr9 gene in comparison to wild type animals. In contrast, treatment with a TLR9 agonist led to an improved clinical outcome. Remarkably, <i>in vitro</i> formation of osteoclasts appeared to be slightly enhanced in cells isolated from TLR9<sup>–/–</sup> mice compared to those from wild type animals. Moreover, osteoclastogenesis was reduced by ∼60% in cells from wild type animals grown in the presence of the TLR9 agonist whereas, as expected, no effect was seen in cells from TLR9<sup>–/–</sup> animals. <h3>Conclusions</h3> These results suggest that TLR9 might play a beneficial regulatory role in the effector phase of erosive autoimmune arthritis by negatively affecting differentiation and activation of bone resorbing osteoclasts. Nevertheless, the precise role of TLR9 in the different stages of arthritis needs to be further elucidated. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4243